Epidemiological and experimental animal studies have strongly indicated that the risk of breast cancer development is influenced by the level of lipids in the diet. Current evidence suggests that this effect of fat is manifest directly at the breast locus. Experiments with intact animals and with cultured epithelium or breast explants, have led to the formulation of a model in which the prolactin stimulated breast epithelium recruits fatty acids needed for growth from proximal fat cells. Prolactin triggers the release of histamine either from mast cells in the mammary gland or from the epithelium itself. Histamine then activates the neighboring fat cell's lipases with the consequent release of fatty acids. The prolactin primed epithelium then selectively takes up the unsaturated fatty acids, part of which become localized in membrane phospholipids, favoring proliferation by as yet, undefined means. Elevations in dietary fat above the buffering capacity of the mammary adipocytes may thus directy sypply the stimulating fatty acids to the mammary epithelium bypassing the required recruitment step, which may be rate limiting for proliferation.